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Evolution of Borrelia burgdorferi

The Borrelia burgdorferi sensu lato (s.l.) species complex currently consists of 18 species (Margos et al. 2010; Rudenko et al. 2009a, 2009b). Of these 18 genomic species, three are confirmed etiologic agents of Lyme disease: Borrelia burgdorferi sensu stricto, Borrelia afzelii, and Borrelia garinii (Stanek and Reiter, 2011). All of them are linked to Lyme disease in Europe, whereas only B. burgdorferi is present in North America. So how did all of these Borrelia species come to exist? Were there always 18 of them, or did they all stem from the same origin? And, if so, where did it all begin? These are the questions we’ll be addressing in this blog.

It all began in Europe. Margos et al (2008) found that B. burgdorferi originated in Europe rather than in North America as previously proposed (Marti et al. 1997). The bacteria, however, have been present in North America since about one million years ago (Hoen et al. 2009). This indicates a prehistoric spread of B. burgdorferi in both North America and Europe, long before the emergence of modern Lyme disease (1970’s). Additionally, the spread of B. burgdorferi within North America went in an east-west direction, beginning in the northeast (Hoen et al. 2009). Potential explanations for how the bacterium got to the northeast in the first place include migrating birds, as B. burgdorferi has been found in birds from both continents (Ginsbert et al. 2005; Comstedt et al. 2006).


During European colonization and industrial development in North America, deforestation and unregulated hunting (especially on deer) led to a drastic decrease in the bacterium’s vector (Ixodes scapularis; Halls 1984). As the geographic range and abundance of both vectors and hosts decreased, so did B. burgdorferi’s population size. This led to a decrease in the spirochete’s genetic diversity due to genetic drift, which is especially effective on smaller population sizes (Qiu et al. 2002; Kliman et al. 2008). Researchers believe that some of their genetic diversity has been regained, however, since the reforestation of much of the eastern US during the mid-20th century (Spielman et al. 1985). Reforestation led to a massive increase in the geographical range of I. scapularis, which also coincides with the modern emergence of Lyme disease.

There is still relatively little genetic heterogeneity in the B. burgdorferi’s genome compared to other Borrelia species/strains (Qiu et al. 2002). The diversity that does exist generally arises due to mutation, recombination, and natural selection. Since B. burgdorferi is such a slow-growing bacterium, however, their mutation rate is very low (Hoen et al. 2009). Genes often used to differentiate between different Borrelia species include the outer surface protein (osp) encoding loci (Bunikis et al. 2004; Girard et al. 2009; Margos et al. 2011). As mentioned in the previous blog posts, ospA aids in tick-spirochete interactions while ospC is important for spirochete-host interactions (Schwan et al. 1995; Pal et al. 2000; Schwan and Piesman, 2000; Pal et al. 2004). Different ospA genes among Borrelia species may be a result of differential adaptation to genetically different ticks. For example, B. burgdorferi produces different ospA proteins than Borrelia bissettii, a Borrelia strain from Colorado (Postic et al. 1998; Postic et al. 2007). The main vector for B. bissettii is Ixodes spinipalpis, which is genetically different from I. scapularis (Burkot et al. 2001). Similarly, infecting different hosts requires the expression of slightly different ospC proteins (Brisson and Dykhuizen, 2004). For example, B. afzelii is specialized on rodent hosts and is killed by the complement system of birds, whereas B. garinii is specialized on avian hosts and is killed by the complement system of rodents (Kurtenbach et al. 1998, 2002).

Borrelia burgdorferi is currently the only Borrelia species causing Lyme disease in North America. There is a possibility, however, that B. garinii may be making its move over the ocean. Smith et al (2006) found B. garinii in seabird ticks (Ixodes uriae) along the Atlantic coast of North America (Canada and Maine). We do not yet know whether or not this spirochete will become the next etiologic agent of Lyme disease in North American for humans. (But we hope not as B. garinii is the most neurotropic of the three genospecies that cause Lyme disease!)


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References

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